The herbicide 2,4-dichlorophenyl-p-nitrophenyl ether (TOK-R) has been demonstrated to induce respiratory distress in newborns with in utero exposure. Many of the clinical manifestations of respiratory distress syndrome (RDS) are apparent without any measurable effects on surfactant synthesis. The sensitive period in rodent gestation to TOK-induced lung damage is days 9-11 of development, when the lung rudiment is first formed. We propose to examine the mechanism of action of the compound, and to more fully explore its effect on developing rodents' lungs. In particular, we wish to ascertain whether the compound is preferentially accumulated or metabolized in developing lungs; whether the compound induces structural malformations in the formation of the tracheobronchiolar tree and alveoli, or in deposition of connective tissue in the lung rudiment; and whether alterations in static and dynamic compliance, pulmonary resistance and functional residual capacity of the lung can be demonstrated in offspring surviving low dose exposure in utero. In this manner, we hope to elucidate some of the basic processes of lung maturation, and to more completely elucidate the etiology of RDS.